Current Role at Stanford

Life Science Research Professional -1

Honors & Awards

  • Virtual Travel Award, Society for Basic Urology Research, Inc. (November, 2020)

Education & Certifications

  • Certificate, University of California Santa Cruz, Biotechnology (2017)
  • MS, Istanbul Technical University, Molecular Bology and Genetics, Biotechnology (2008)
  • BS, Istanbul Technical University, Molecular Biology and Genetics (2006)


  • A novel oncogene-mediated metabolic gene signature predicts breast cancer outcome, Stanford University


    Palo Alto, California


All Publications

  • Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1. Proceedings of the National Academy of Sciences of the United States of America Hsu, E. C., Rice, M. A., Bermudez, A., Marques, F. J., Aslan, M., Liu, S., Ghoochani, A., Zhang, C. A., Chen, Y. S., Zlitni, A., Kumar, S., Nolley, R., Habte, F., Shen, M., Koul, K., Peehl, D. M., Zoubeidi, A., Gambhir, S. S., Kunder, C. A., Pitteri, S. J., Brooks, J. D., Stoyanova, T. 2020


    Resistance to androgen deprivation therapy, or castration-resistant prostate cancer (CRPC), is often accompanied by metastasis and is currently the ultimate cause of prostate cancer-associated deaths in men. Recently, secondary hormonal therapies have led to an increase of neuroendocrine prostate cancer (NEPC), a highly aggressive variant of CRPC. Here, we identify that high levels of cell surface receptor Trop2 are predictive of recurrence of localized prostate cancer. Moreover, Trop2 is significantly elevated in CRPC and NEPC, drives prostate cancer growth, and induces neuroendocrine phenotype. Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppresses these abilities in vivo. Trop2-driven NEPC displays a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor growth and metastatic colonization and reverse neuroendocrine features in Trop2-driven NEPC. Our findings establish Trop2 as a driver and therapeutic target for metastatic prostate cancer with neuroendocrine phenotype and suggest that high Trop2 levels could identify cancers that are sensitive to Trop2-targeting therapies and PARP1 inhibition.

    View details for DOI 10.1073/pnas.1905384117

    View details for PubMedID 31932422

  • Discovery of PTN as a blood-based biomarker of pro-metastatic prostate British Journal of Cancer Liu, S., Shen, M., Hsu, E., Zhang, A., Garcia-Marques, F., Nolley, R., Koul Koul, K., Rice, M., Aslan, M., Pitteri, S., Massie, C., George, A., Brooks, J., Gnanapragasam, V., Stoyanova, T. 2020
  • Plectin is a Regulator of Prostate Cancer Growth and Metastasis Oncogene Buckup, M., Rice, M., Hsu, E., Marques, F., Liu, S., Aslan, M., Bermudez, A., Huang, J., Pitteri, S., Stoyanova, T. 2020
  • Loss of Notch1 activity inhibits prostate cancer growth and metastasis and sensitizes prostate cancer cells to anti-androgen therapies. Molecular cancer therapeutics Rice, M. A., Hsu, E. C., Aslan, M., Ghoochani, A., Su, A., Stoyanova, T. 2019


    Prostate cancer remains among the leading causes of cancer-related deaths in men. Patients with aggressive disease typically undergo hormone-deprivation therapy. While treatment is initially very successful, these men commonly progress to lethal, castration resistant prostate cancer in 2-3 years. Standard therapies for castration resistant prostate cancer include second-generation anti-androgens, which prolong patient lifespan by only several months. It is imperative to advance our understanding of the mechanisms leading to resistance to identify new therapies for aggressive prostate cancer. This study identifies Notch1 as a therapeutic target in prostate cancer. Loss of Notch1 in aggressive prostate cancer cells decreases proliferation, invasion and tumorsphere formation. Therapeutic inhibition of Notch1 activity with gamma secretase inhibitors RO4929097 or DAPT in prostate cancer cells further results in decreased proliferative abilities. Loss of Notch1 and treatment of immunocompromised mice bearing prostate cancer xenografts with RO4929097 display significantly impaired tumor growth. Loss of Notch1 additionally decreased metastatic potential of prostate cancer cells in invasion assays in vitro as well as in vivo experiments. Moreover, treatment with gamma secretase inhibitors, or Notch1 gene deletion synergized with anti-androgen therapies, Enzalutamide or Abiraterone, to decrease the growth of prostate cancer cells. Combination of gamma secretase inhibitors with Abiraterone significantly inhibited cell migration and invasion, while combination with Enzalutamide reversed Enzalutamide induced migration and invasion. These collective findings suggest loss of Notch1 delays growth of CRPC, inhibits metastasis, and inhibition of Notch1 activation in conjunction with second-generation anti-androgen therapies could delay growth and progression of prostate cancer.

    View details for PubMedID 31028097

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